The mechanisms by which the lung undergoes inflammatory injury are poorly understood. One important mediation system in the establishment of inflammatory lung disease may be the components of the Hageman factor activated systems. The objective of this proposal is to define in quantitative terms the role of the Hageman factor activated systems in inflammatory injury to the lung. The approach to this problem is to first establish a model of inflammatory injury which can produce both non-immunologic and immunologic injury. Kaolin, coated with antigenic proteins, will be injected into the lungs of normal and sensitized rabbits. Injury will be assessed by histologic and biochemical changes. The participation of members of the Hageman factor activated systems will be measured by immunofluorescence and by accumulation of radiolabeled precursor components at the site of the lesion. The effect of specific inhibition of components of the Hageman factor systems with concurrent assessments of injury will provide evidence for the direct participation of these mediators in inflammatory injury to the lung. This proposal will provide evidence for the participation of one mediation system in the development of inflammatory injury to the lung and will contribute to our understanding of the pathogenesis of human lung disease.